Role of Stress Protein on Bacterial Infection
Role of Stress Protein on Bacterial Infection
批准号:
08670317
负责人:
YAMAMOTO Tomoko
金额:
$1.47万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
1996
资助国家:
日本
项目状态:
已结题
起止时间:
1996 至 1998
中文摘要
所有生物体对不利条件如应激环境的反应是通过快速和短暂地加速一组称为应激蛋白的蛋白质的合成。对于病原菌,巨噬细胞的细胞内环境是最恶劣的环境之一。因此,吞噬细胞中的细菌可能通过应激蛋白的表达来响应有害刺激,而那些促应激蛋白的表达可能是有害刺激的一部分。teiris可以使胞内细菌在吞噬细胞中的存活处于优势。为了阐明细菌应激蛋白对巨噬细胞存活和毒力表达的作用,我们研究了小肠结肠炎耶尔森菌和单核细胞增生李斯特菌在巨噬细胞吞噬后的应激反应和应激蛋白的作用。结果如下:(1)小肠结肠炎耶尔森氏菌gsrLAMBDA在巨噬细胞中被鉴定为在细胞外环境应激和细胞内应激下由于吞噬作用而保护细胞所必需的。gsrLAMBDA编码碱性49.5kDa蛋白,其为周质蛋白酶。(2)GsrA应激蛋白由巨噬细胞吞噬诱导。(3)单核细胞增生李斯特菌在没有应激蛋白诱导的情况下可以在巨噬细胞中生长。(4)为了了解应激蛋白DnaK对单核细胞增生李斯特菌细胞内存活的作用,克隆了dnaK基因并进行了分子分析。(5)DnaK对巨噬细胞中嗜酸细胞增生李斯特菌的生存没有很大贡献,但参与吞噬步骤。从这些结果可以推测,除了种特异性机制之外,与胁迫蛋白的共同机制也有助于细菌病原体esis的表达。
英文摘要
All organisms respond to unfavorable conditions such as stressful environment by the rapid and transient acceleration in the synthesis of a group of proteins called the stress proteins. For pathogenic bacteria, the intracellular environment of macrophages is one of the most hostile environments. Therefore, the bacteria in the phagocytes may respond to the hostile stimuli by the expression of the stress proteins, and those pro. teiris may put the intracellular bacteria at advantages in the survival in the phagocytes. To elucidate the role of bacterial stress protein on the survival in the macrophages and expression of virulence, we studied the stress response and the role of stress proteins of Yersinia enterocolitica and Listeria monocytogenes within macrophages after phagocytosis. The results are as follows ; (1) The Y.enterocolitica gsrLAMBDA was identified as essential for protecting cells under both extracellular environmental stress and intracellular stress in macrophages due to phagocytosis. The gsrLAMBDA encodes a basic 49.5 kDa protein which is a periplasmic protease. (2) The GsrA stress protein was induced by macrophage phagocytosis. (3) L.monocylogenes could grow in macrophages without the induction of stress proteins. (4) The dnaK gene was cloned and subjected to the molecular analysis to understand the role of stress protein DnaK for intracellular survival of L.monocylogenes . (5) The DnaK does not largely contribute to the survival of L.inonocytogenes in macrophage cells but is involved in the step of the phagocytosis. From these results, it is speculated that common mechanisms with the stress proteins would contribute to the expression of the bacterial pathogen esis besides the species-specific mechanisms.
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Yamaguchi H et al.: "Induction and epitope analysis of heat shock protein of Helicobacter pylori." J.Gastroenterol.31. 12-15 (1996)
Yamaguchi H 等人:“幽门螺杆菌热休克蛋白的诱导和表位分析。”
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通讯作者:
山本 友子: "細菌の食菌抵抗性とストレス蛋白質" 医学のあゆみ. 178. 446-447 (1996)
Tomoko Yamamoto:“细菌食物抗性和应激蛋白”医学史 178. 446-447 (1996)。
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Yamaguchi H et al.: "Analysis of the epitopes recognized by mouse monoclonal antibodies directed to Yersinia enterocolitica heat-shock protein 60." Microbiol.Immunol.40. 77-80 (1996)
Yamaguchi H 等人:“针对小肠结肠炎耶尔森氏菌热休克蛋白 60 的小鼠单克隆抗体识别的表位的分析。”
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Tomoko Yamamoto, Tomoko Hanawa and Shigeru Kamiya: "The Yersinia enterocolitica GsrA protein, involved in intracellular survival, is induced by macrophage-phagocytosis" Infect.Immun. 65. 2190-2196 (1997)
Tomoko Yamamoto、Tomoko Hanawa 和 Shigeru Kamiya:“小肠结肠炎耶尔森氏菌 GsrA 蛋白参与细胞内存活,由巨噬细胞吞噬作用诱导” Infect.Immun。
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